Verapamil is an important anti-anginal drug which dilates coronary arteries and decreases the work of the heart. We have previously shown that this drug can reduce the severity of ischemic injury after coronary artery occlusion without changing coronary blood flow. It has been noted that calcium channel blockers, such as verapamil, can reduce the peak level of coronary blood flow which occurs during the reactive hyperemia which follows after releasing a temporary coronary artery occlusion. It seemed reasonable that this reduction in the peak coronary blood flow repayment upon release of a total coronary occlusion, would be related to the reduction in the severity of the ischemic stimulus which had occurred during the previous occlusion. We tested this in a group of dogs and confirmed that the peak coronary blood flow during their active hypermia was, indeed, reduced by about 40%. Surprisingly, we found that the peak coronary blood flow which occurred in response to an intracoronary infusion of adenosine was also reduced by about 30%. Thus the reduction in peak coronary vasodilator reserve after verapamil cannot be explained simply by a reduced severity of the ischemic stimulus for vasodilation. Rather it appears that verapamil has a potentially adverse effect to inhibit maximum coronary vasodilator reserve, in response to stress.